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- W2014040910 abstract "Pancreatic cancers have an intense resistance to currently available therapeutics which results in a dismal 5-year survival rate. This resistance points toward altered cell survival and metabolic pathways. In this regard we have previously shown that pancreatic cancers have elevated basal autophagy, which is required for their continued growth. Importantly, inhibition of autophagy pharmacologically or by RNAi approaches leads to decreased oxidative phosphorylation, a drop in ATP production, and ultimately growth inhibition. These findings have implicated autophagy as a key component of pancreatic cancer metabolism and have motivated the opening of multiple clinical trials assessing the efficacy of hydroxychloroquine as an autophagy inhibitor in pancreatic cancer. Additional work from our group has demonstrated that oncogenic Kras promotes a systematic rewiring of pancreatic cancer metabolism allowing glucose and glutamine to be utilized in a variety of biosynthetic pathways. Importantly, several of these metabolic pathways are critical for tumor growth and therefore represent potential therapeutic targets. These and other aspects of pancreatic cancer metabolism will be discussed.Citation Format: Jaekyoung Son, Costas A. Lyssiotis, Shenghong Yang, Haoqiang Ying, Xiaoxu Wang, Lewis C. Cantley, Alec C. Kimmelman. Autophagy, metabolism, and pancreatic cancer. [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer: Progress and Challenges; Jun 18-21, 2012; Lake Tahoe, NV. Philadelphia (PA): AACR; Cancer Res 2012;72(12 Suppl):Abstract nr IA14." @default.
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- W2014040910 date "2012-07-15" @default.
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- W2014040910 title "Abstract IA14: Autophagy, metabolism, and pancreatic cancer." @default.
- W2014040910 doi "https://doi.org/10.1158/1538-7445.panca2012-ia14" @default.
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